Electrolyte abnormalities Flashcards
Diabetes insipidus (DI).
a) Two main types and causes of each
b) Clinical features
c) Investigations
d) Management
e) Differentiating DI from primary polydipsia
a) Cranial.
- mechanism: inadequate production of ADH
- causes: idiopathic, head injury, pituitary tumour or surgery, hypothalamic dysfunction, Sheehans syndrome, inflammation (eg. sarcoid, GBS)
Nephrogenic
- mechanism: defect in AQP channels/ V2 receptors
- causes: CKD, lithium, hypercalcaemia, inherited
b) Polyuria, polydipsia, dehydration, hypernatraemia, raised serum osmolality and reduced urine osmolality
c) - Urine: osmolality, dip (?glucose)
- Bloods: serum osmolality, U+Es, glucose, calcium (differential - hypercalcaemia)
- Water deprivation test (shows inadequate concentration of urine)
- Then add desmopressin to distinguish cranial from nephrogenic DI (cranial: AVP leads to urine concentration)
- If cranial cause suspected - MRI pituitary/hypothalamus
d) Cranial - desmopressin nasal spray or tablets
Nephrogenic - conservative? - increase fluid intake
e) Primary (psychogenic) polydipsia - patients are able to concentrate their urine on water deprivation testing (rise in urine Osm and reduction in serum Osm)
Requirements per day.
a) Sodium
b) Potassium
c) Water
d) Adequate urine output (per hour)
e) Glucose
a) 1 mmol/kg/day
b) 1 mmol/kg/day
c) 25 - 30 ml/kg/day (~ 1 ml/kg/hr)
d) > 0.5 ml/kg/hr (~ 30 - 40 ml/hr)
e) 50–100 g/day
-
-
Body fluid.
- 70 kg man (if 60% body mass is water), calculate:
a) Total body fluid (L)
b) Intracellular fluid (L)
c) Extracellular fluid (L) - split into interstitial and intravascular
70 kg man
x 0.6 = 42 L total body water
2/3 is intracellular = 28 L
1/3 is extracellular = 14 L
Of the extracellular,
- 75% is interstitial = 10 L
- 25% is intravascular = 4 L
Water balance: regulating mechanisms
Raised plasma osmolality:
- Detected by osmoreceptors in hypothalamus
- Thirst response - drink more water
- Vasopressin secreted by posterior pituitary
- Attaches to V2 receptors in collecting ducts of kidneys
- AQP-2 channel up-regulation in collecting ducts
- Increased water reabsorption (reduced excretion)
- Reduces plasma osmolality
Osmolality.
a) What is it? (units)
b) Equation
c) Normal range
a) Concentration of solute (mOsm) per kg of water
b) 2x [Na+] + urea + glucose
c) Normal Osmolality = 282 - 295 mOsmol/kg
d)
Osmolality.
a) High plasma, high urine
b) High plasma, low urine
c) Low plasma, high urine
d) Low plasma, low urine
a) Dehydration (hypernatraemic)
b) Diabetes inspidus (hypernatraemic)
c) SIADH (hyponatraemia)
d) Primary polydipsia, fluid overload (hyponatraemia)
Hyponatraemia: aetiology
- 3 distinctions, with main causes for each
- Hypovolaemic (dry, tachy, low BP, etc.)
- Low urinary Na+:
• Vomiting + diarrhoea
• Burns
• Pancreatitis
- High urinary Na+ (salt-wasting): • Diuretics • Addison’s (or occasionally pituitary failure) • Cerebral salt wasting • Salt wasting nephropathy
- Euvolaemic:
- Acute water load / primary polydipsia
- Hypothyroid
- SIADH
- Low glucocorticoid (non-salt wasting) - Hypervolaemic (raised JVP, oedema, etc.)
• Cirrhosis of liver/liver failure
• CCF
• CKD / nephrotic syndrome
Hyponatraemia: clinical features
a) Severity depends on what 2 factors?
b) Possible features
a) Speed of onset; severity of hyponatraemia
b) - asymptomatic, or…
- Mild: • headache, • lethargy, • anorexia and abdominal pain, • weakness, • confusion
- Severe: • delirium/hallucinations, • agitation • seizures • decreased conscious level • coma
Hyponatraemia: investigations
a) Urine
b) Blood
c) Special tests
d) If SIADH suspected - 2 Ix?
a) Urinary electrolytes (eg. sodium), osmolality, glucose, protein, cortisol
b) Plasma osmolality, glucose, U+Es, TSH, cortisol, LFTs
c) - If cortisol low - synacthen test
d) CXR and CT head (usually chest and brain causes)
Acute hyponatraemia: management
acute is < 24 hour duration
Rapid hypertonic saline replacement.
- Manage in HDU/ITU setting
- 150 ml of 3% NaCl given IV over 15 mins
- Repeat if no response
- Monitor U+Es, etc.
- Aim for no more than 10 mmol/L increase per 24 h
Chronic hyponatraemia: management (> 24 hour duration)
- general management
- Hypovolaemic vs. euvolaemic vs. hypervolaemic
- complication of replacing sodium too quickly
General management.
- stop any precipitants (eg. diuretics)
- Treat the underlying cause
Hypo.
- IV NaCl 0.9%
Euvolaemic/hyper.
- Fluid restrict
Complication of rapid correction.
- Central pontine myelinolysis - leads to quadriplegia, locked in syndrome, etc.
SIADH.
a) Causes
b) 3 criteria to diagnose
c) Clinical fx
d) Suspect in anyone with cancer who has what electrolyte abnormality?
e) Investigations and management
a) Mainly pulmonary, CNS, malignant and drug-induced causes. SIADH:
- Small cell lung cancer/other malignancy (eg brain mets)
- Infection (pneumonia, TB, HIV)
- (sub)Arachnoid haemorrhage (and other CNS - head injury, SOL, meningitis, GBS, MS)
- Drugs: diuretics, SSRIs, ACEIs, PPIs
- Hereditary (rare)
b) - Euvolaemic hyponatraemia
- Low serum osmolality and raised urine osmolality
- Normal thyroid and adrenal function
c) - Often asymptomatic
- Hyponatraemia: anorexia, headache, cramps, nausea, vomiting, lethargy. Severe: reduced GCS, seizures
d) Hyponatraemia
e) - Investigate for cause (if unknown): CT TAP / CT head
- Treat underlying cause
- 1st line: fluid restriction
- 2nd line: demeclocycline (blocks ADH and induces partial nephrogenic diabetes insipidus)
- 3rd line: vaptans (eg, tolvaptan): vasopressin V2 receptor antagonists
A 28 year old man has an road traffic accident, with severe head injury. Unconscious, blood noted in external auditory meatus. Wakes up very thirsty, and within 24 hours is producing 6 litres of urine/day
• Serum sodium 154mmol/l
a) Likely diagnosis
b) How is it differentiated from diabetes mellitus?
c) What other investigations would you do?
a) Diabetes insipidus (cranial)
b) No glycosuria, no hyperglycaemia
c) - Urine: dip, osmolality, collection (total urine output: will be > 3L in DI)
- Serum: osmolality, calcium, glucose, U+Es, LFTs
- Imaging: CT head/ ?MRI pituitary
- Special tests: water deprivation test (+ desmopressin)
Hypernatraemia.
a) Main causes
b) Clinical features
c) Investigations
d) Management - general
e) Specific in DI
a) - Dehydration - inadequate intake, thirst impairment (eg. dementia), excessive water loss
- Diabetes insipidus
- Inappropriate diuresis or laxatives
- Watery diarrhoea/ excessive sweating
b) - Dehydration: thirst (+ polyuria in DI), dry
- CNS: lethargy, weakness, confusion, irritability, myoclonic jerks, seizures, coma
c) - Urine: dipstick
- Blood: U+E, calcium, glucose
?lithium levels
- Urine and plasma osmolality if DI suspected
- ?CT head if DI suspected
d) - Treat underlying cause
- Stop any precipitants (eg. loop diuretics, osmotic laxatives)
- Correct imbalance using hypotonic saline (0.45% NaCl)
- If acute - rapid correction
- If chronic - slow correction
e) - Nephrogenic (increase fluids)
- Cranial (desmopressin nasal spray)
Hypokalaemia.*
a) Definition and severity grading
b) Causes
c) Clinical features
*Probably the most common electrolyte abnormality affecting hospitalised patients
a) Defined as a serum K+ < 3.5
- Mild - 3.1 - 3.5 mmol/L
- Moderate - 2.5 - 3.0 mmol/L
- Severe - <2.5 mmol/L
b) 1. Excessive loss through:
- Kidneys - diuretics* (thiazide, loop), RTA, low Mg2+**, hyperaldosteronism, Bartter’s/Gitelman’s
- GI tract (vomiting, diarrhoea or laxative abuse)
- Skin/other - sweating, burns
- Potassium-sparing diuretics cause HYPERkalaemia:
- Aldosterone antagonists (spiro, eplerenone)
- Amiloride
**Hypomagnesaemia (magnesium required for K+ secretion into the urine via Na/K/ATPase channel)
- Inadequate intake:
- IV fluids without potassium addition
- Anorexia/malnutrition
- TPN feeds - Transcellular shift
- Insulin*
- Salbutamol*
- Alkalosis
***May be as treatment for HYPERkalaemia
c) - Mild-mod: asymptomatic, weakness, lethargy, constipation
- Severe: severe neuromuscular weakness, ascending paralysis, respiratory failure, ileus, tetany, arrhythmias
Hypokalaemia: investigations and management
- Bloods, urine, special tests
- ECG changes
- Management (mild)
- Management (severe)
Bloods.
- U+E (low Na+ suggests diuretics or volume depletion)
- Acid-base (?hypokalaemic alkalosis),
- Magnesium (low Mg often accompanies hypokalaemia and must be corrected to enable recovery of serum K+).
- Glucose, LFTs, etc.
Urine.
- Low K+ suggests GI loss
- High K+ suggests renal loss
- Urinary Na+ and osmolality
ECG.
- QT prolongation
- Flat T waves (opposite of hyperkalaemia)
- ST depression
- Prominent U waves
- Arrhythmias; AF, VT, Torsades, VF, etc.
Special tests.
- Renin:aldosterone test
- Urine and plasma osmolality
- Cortisol - ?Cushing’s
- Renal USS - ?RAS
Management (mild).
- Dietary - banana (12 mmol K+), other fruit + veg
- Oral supplements - Sando-K (dissolved in water), Kay-Cee-L (liquid form)
- KHCO3 if hypokalaemia and acidosis (eg. RTA)
- Magnesium replacement (magnesium aspartate) may be required if hypoMg2+ to allow for K+ renal reabsorption
Management (severe).
- IV potassium chloride (KCl), slow infusion* (may first require magnesium supplementation)
- Should not exceed 10 mmol/hr via peripheral line (higher rates would need to be via CVC)
- Give in bag of NaCl** (20 mmol in 500 ml = 40 mmol/L) over at least 2 hours
- Cardiac monitoring, and bloods every 1 - 3 hours
- Once ECG and clinical signs improve (weakness, fatigue, etc.), consider reducing rate and/or switching to oral supplements
*NEVER give KCl stat (lethal injectio - arrhythmias)
** Don’t give with dextrose, as this will lead to insulin release, which will worsen hypokalaemia
Hyperkalaemia.
a) Potassium metabolism
b) Causes
c) Presentation
d) Grading of severity
a) - Intake - dietary
- Loss - renal excretion (90%) and GI loss (10%)
- Predominantly intracellular ion
b) Reduced excretion.
- Renal failure - AKI, CKD, RTA
- Low aldosterone - drugs (ACE, ARBs, spiro, amiloride - beware these drugs in combination!), Addison’s disease
Increased potassium intake.
- Sando-K
- KCl infusion
Intracellular release.
- Acidosis (eg. DKA)
- tumour lysis
- rhabdomyolysis
Pseudohyperkalaemia.
- Sample faults - prolonged tourniquet time, haemolysed sample, clenched fist, from limb receiving IV KCl, etc.
c) - Often asymptomatic
- May have weakness, palpitations, signs of complications (eg, arrhythmia) or cause (eg. AKI)
d) - Mild: 5.5 - 5.9
- Moderate: 6.0 - 6.4
- Severe: 6.5 +
Hyperkalaemia: investigations and results
- bloods
- other
- ECG changes (early, later, severe)
Bloods.
- Repeat U+E if unexpected
- Glucose, ketones, acid-base, etc.
- CK, uric acid, Pi, calcium, etc (?rhabdo, tumour lysis)
Special tests.
- cortisol + synacthen - ??adrenal insufficiency
- renal USS/ biopsy, etc.
ECG.
- Early: Tall, tented T waves (widespread)
- Small/absent/inverted P waves
- PR prolongation (hyPRkalaemia, vs. long QT in hypoK+)
- Severe: broad QRS (> 120 ms), AV block, RBBB/LBBB, fatal arrhythmias
Hyperkalaemia: management
a) What 2 main things dictate management strategy?
b) General principles
c) Management to reduce K+
d) Management to protect heart
e) Resistant hyperkalaemia - management
Must consider:
- ECG changes (yes = must protect heart)
- Potassium (> 6.5 = must protect heart)
General principles.
- Stop any precipitating factors (eg. ACE, NSAIDs, spiro, Sando-K)
- Treat treatable causes (eg. fluids, hydrocortisone)
- Protect the kidneys
- Protect the heart
- Reduce serum potassium (intracellular shift and increased excretion/reduced absorption)
Management (no ECG changes, K+ < 6.5):
- IV 10U insulin (ActRapid), and
- 250ml 10% glucose (over 15 - 30 mins)
- Re-check potassium at 2- 4 hours (give 2 doses before escalating)
- Calcium resonium (binds K+ in the large intestine to increase faecal excretion)
- Salbutamol nebs (beware tachycardia)
- Diuretics if overloaded (beware AKI)
Management (ECG changes, or K+ > 6.5):
- IV 10 mls 10% calcium gluconate: increases the cardiac threshold potential, stabilising the cardiac membrane
- repeat ECG
- Give another 10 ml every 10 mins (up to 50 ml) if no effect on ECG
- above measures to reduce hyperK+
- (alternative to Ca-Gluc: CaCl or hypertonic saline)
Resistant hyperkalaemia.
- Discuss with renal physicians
- Consider haemodialysis
- Consider sodium bicarbonate (don’t mix with calcium - forms calcium carbonate = chalk)
- Consider diuretics if overloaded (beware AKI)
Calcium homeostasis.
a) Active and inactive calcium
b) Hormonal regulation
a) Calcium levels.
- About 50% bound to albumin = inactive
- Ionised (unbound) calcium = active
- Low albumin = higher unbound (active) calcium
- Corrected calcium corrects for albumin levels
b) Homeostasis.
- Low calcium - activates PTH
- PTH leads to increased Ca2+ reabsorption (and reduced Pi reabsorption) in DCT and collecting ducts
- PTH activates osteoclasts to increase bone resorption
- PTH activates vitamin D production, which increases absorption of calcium in gut
Hypocalcaemia.
a) Define
b) Causes
c) Presentation - mild and severe (everything spasms)
d) Investigations
e) ECG changes
f) Management
a) Corrected calcium < 2.12
(Severe < 1.9)
b) Hypoparathyroidism.
- Iatrogenic (previous thyroid surgery, central lines, etc.)
- Congential (agenesis, DiGeorge)
Other (will have high PTH - secondary hyperPTH)
- Vitamin D deficiency
- Renal failure
- Hypomagnesaemia
- Drugs - calcium chelators, bisphosphonates
- Acute pancreatitis
- Tumour lysis/ rhadbomyolysis
c) - Paraesthesia (fingers, toes, peri-oral), muscle cramps
- Severe: tetany, carpopedal spasm, laryngospasm, bronchospasm, seizures, arrhythmias
- Signs: Chvostek and Trousseau’s signs
d) - Bloods: U+E, corrected calcium, magnesium, phosphate, PTH, vitamin D; creatine kinase, uric acid, etc.
- ECG
e) ECG changes:
- prolonged QT
- arrhythmias
f) - Treat where symptomatic, or severe (Ca2+ < 1.9)
- 10 mls calcium gluconate 10% - slow IV injection
- Observe ECG and repeat if necessary
- If hypomagnesaemic - correct this to allow for calcium correction
- Oral - calcium and vitamin D supplements (AdCal)
Hypercalcaemia.
a) Define
b) Causes
c) Clinical features
d) Investigations
e) Management
b) Malignant.
- osteolytic (bone mets, myeloma)
- ectopic PTH-related peptide production (e.g. SCC)
Primary hyperparathyroidism*.
- primary (mainly post-menopausal women; adenoma most commonly),
- Note: secondary (kidney, liver, bowel disease causing low Ca2+) and tertiary (CKD) hyperparathyroidism usually have normal or low calcium
Other.
- Vitamin D toxicity
- Drugs - thiazide diuretics, lithium
- Granulomatous conditions (eg. sarcoid, TB)
- Familial hypocalciuric hypercalcaemia
b) Bones, moans, groans, stones, thrones…
- Acute (mild-mod): thirst, polyuria, confusion, constipation, fatigue, weakness
- Acute severe: acute abdomen, pancreatitis, arrhythmia, coma
- Chronic: depression, constipation, calcium deposits: nephrocalcinosis, nephrolithiasis, chondrocalcinosis (pseudogout)
d) - ECG: short QT (opposite of hypoCa2+), arrhythmias
- Bone profile: corrected calcium, phosphate, Alk Phos, albumin (add PTH)
- Imaging: XR affected bones (pepperpot skull in myeloma), ?CT KUB
e) - Uncorrected serum calcium measurement measures both unbound and bound calcium.
- Only unbound (ionised) calcium is physiologically active; the rest is inactive and bound to albumin.
- If albumin is low, the unbound (active) calcium will be raised; hence, corrected calcium accounts for low/raised albumin levels
e) - Asymptomatic/non-severe: consider ‘watch and wait’
- Manage AKI: fluids (0.9% NaCl) + furosemide if overload
- 1st line: IV bisphosphonates (eg. zoledronic acid)
- 2nd line: denosumab
- Treat underlying cause (if hyperPTH - consider partial parathyroidectomy)
